A mechanism study of meloxicam in preventing chronic rotator cuff injury

AERKEN Aikeremujiang; GE Yun-lin; DING Shu-chen; WANG Zhe-yang; LIU Zhi-rong; WANG Da-wei; JIN Xiao-jun; CHEN Li-ying

doi:10.3969/j.issn.2095-252X.2017.12.014

Abstract：Objective To investigate the mechanism of meloxicam in preventing chronic rotator cuff injury. Methods A total of 36 rats were randomly and evenly divided into the model group, meloxicam group and normal control group ( n = 12 ). Model group and meloxicam group received bilateral modeling surgery, while the normal control group not. All rats were exposed to 30 minutes of downhill running at the speed of 17 m / min ( -13.5° ) every day at the fourth day after the operation. Meloxicam group received meloxicam ( concentration of 3 mg / ml ) subacromial injection at the third week, the fourth week and the fifth week after the modeling, 0.3 ml each time. Model group and the normal control group were injected with 0.3 ml saline at the same time. All rats were sacrificed at the sixth week and bilateral shoulder specimens were collected. For each rat, one shoulder was randomly selected to receive HE, Masson and PGE2 immunohistochemical staining. The other shoulder was used to detect BMP-2 expression level with Western-blot technology after the biomechanical testing. Results HE and Masson staining: each group showed no inflammatory cell infiltration; full-thickness tear could be found in all cases in the model group, with severe fiber layering; partial tendon tear and lighter collagen layering could be observed in the meloxicam group; infraspinatustendon in the normal control group was smooth and continuous, no obvious abnormalities. The expressions of PGE2 in the model group were significantly higher than those in both the meloxicam group and the normal control group ( P < 0.001 ). Meloxicam group was compared with the control group, PGE2 showed no statistically significant difference ( P = 0.4246 ). The maximal loadings of tendons in the model group ( 17.95 ± 6.689 ) N were significantly lower than those in both the meloxicam group ( 38.95 ± 8.397 ) N and the normal control group ( 71.66 ± 5.3312 ) N ( P < 0.001 ). The maximal loadings of tendons in the meloxicam group were significantly lower than those in the normal control group ( P < 0.001 ). The expressions of BMP-2 in the model group ( 2.0230 ± 0.2042 ) were significantly higher than those in both the meloxicam group ( 0.4508 ± 0.1274 ) and the normal control group ( 0.1458 ± 0.0613 ) ( P < 0.001 ). The expressions of BMP-2 in the normal control group ( 0.1458 ± 0.0613 ) were significantly lower than those in the meloxicam group ( P < 0.001 ). Conclusions PGE2 expression is one of the causes of chronic rotator cuff injury. Meloxicam can prevent or heal chronic rotator cuff injury to some extent by inhibiting PGE2.